Aged patients and experimental animals are more susceptible to infections than young animals. This proposal seeks to explain, at the cellular level, the increased susceptibility of aged mice to infection with the intracellular pathogen, Listeria monocytogenes. Possible abnormalities of macrophages from aged mice--either in their antigen-presenting or effector function--will be examined. Antigen presentation will be studied by co-culturing the macrophages with heat-killed Listeria and competent T cells from young adults in a system known to be controlled by the I region of H-2. Macrophage effector functions will be assayed by examining cytocidal and bactericidal activities following macrophage activation by T cell factors. Furthermore, the regulation of the number of Ia-bearing macrophages in aged and young adult mice will be compared. Aging-related abnormalities in the generation of helper and suppressor T cells will be examined using combinations of cell transfer and cell culture experiments. Finally, attempts will be made to correct the immune response of aged mice by adoptive transfer of appropriate cells or factors from young adult mice.